EGCG (Epigallocatechin Gallate) Cancer Research Results

EGCG, EGCG (Epigallocatechin Gallate): Click to Expand ⟱
Features:
EGCG (Epigallocatechin Gallate) is found in green tea. 100 times more effective than Vitamin C and 25 times more effective than Vitamin E at protecting cells from damage associated with oxidative stress.
EGCG Epigallocatechin Gallate (Green Tea) -Catechin
Summary:
1. Concentration is a factor that could determine whether green tea polyphenols act as antioxidants or pro-oxidants.
2. Poor bioavailability: taking EGCG capsules without food was better.
3. Cancer dosage 4g/day (2g twice per day)? with curcumin may help (another ref says 700–2100 mg/d)
4. EGCG is susceptible to oxidative degradation.
5. “As for the pH level, the acidic environments enhance the stability of EGCG”.
6. “EGCG may enhance nanoparticle uptake by tumor cells”
7. Might be iron chelator (removing iron from cancer cells)
8. Claimed as synergistic effect with chemotherapy ( cisplatin, bleomycin, gemcitabine.
9. May suppress glucose metabolism, interfere with VEGF, downregulate NF-κB and MMP-9, down-regulation of androgen-regulated miRNA-21.
10. Take with red pepper powder, Capsicum ratio 25:1 (based on half life, they did every 4 hr) (chili pepper vanilloid capsaicin).
11. EGCG mediated ROS formation can upregulate CTR1 expression via the ERK1/2/NEAT1 pathway, which can increase the intake of chemotherapeutic drugs such as cisplatin in NSCLC cells and act as a chemosensitizer [58]
12. Matcha green tea has highest EGCG (2-3X) because consuming leaf.
13. EGCG is an ENOX2 inhibitor.
14. Nrf2 activator in both cancer and normal cells. This example of lung cancer show both directions in different cell lines, but both toward optimim level.
Biological activity, EGCG has been reported to exhibit a range of effects, including:
    Antioxidant activity: 10-50 μM
     Anti-inflammatory activity: 20-50 μM
     Anticancer activity: 50-100 μM
     Cardiovascular health: 20-50 μM
     Neuroprotective activity: 10-50 μM

Drinking a cup (or two cups) of green tea (in which one might ingest roughly 50–100 mg of EGCG from brewed tea) generally results in peak plasma EGCG concentrations in the range of approximately 0.1 to 0.6 μM.

With higher, supplement-type doses (e.g., oral doses in the 500 mg–800 mg range that are sometimes studied for clinical benefits), peak plasma concentrations in humans can reach the low micromolar range, often reported around ~1–2 μM and in some cases up to 5 μM.

Reported values can range from about 25–50 mg of EGCG per gram of matcha powder.
In cases where the matcha is exceptionally catechin-rich, the content could reach 200–250 mg or more in 5 g.

-Peak plasma concentration roughly 1 to 2 hours after oral ingestion.
-Elimination half-life of EGCG in plasma is commonly reported to be in the range of about 3 to 5 hours.

Supplemental EGCG
Dose (mg)   ≈ Peak Plasma EGCG (µM)
~50 mg          ≈ 0.1–0.3 µM
~100 mg         ≈ 0.2–0.6 µM
~250 mg         ≈ 0.5–1.0 µM
~500 mg         ≈ 1–2 µM
~800 mg or higher  ≈ 1–5 µM

50mg of EGCG in 1g of matcha tea(1/2 teaspoon)

Studies on green tea extracts have employed doses roughly equivalent to 300–800 mg/day of EGCG. Excessive doses can cause liver toxicity in some cases.

Methods to improve bioavailability
-Lipid-based carriers or nanoemulsions
-Polymer-based nanoparticles or encapsulation
-Co-administration with ascorbic acid (vitamin C)
-Co-administration of adjuvants like piperine (perhaps sunflower lecithin and chitosan) -Using multiple smaller doses rather than one large single dose.
-Taking EGCG on an empty stomach or under fasting conditions, or aligning dosing with optimal pH conditions in the GI tract, may improve its absorption.(acidic environment is generally more favorable for its stability and absorption).
– EGCG is more stable under acidic conditions. In the stomach, where the pH is typically around 1.5 to 3.5, EGCG is less prone to degradation compared to the more neutral or basic environments of the small intestine.
- At neutral (around pH 7) or alkaline pH, EGCG undergoes auto-oxidation, reducing the effective concentration available for absorption.
– Although the stomach’s acidic pH helps maintain EGCG’s stability, most absorption occurs in the small intestine, where the pH is closer to neutral.
– To counterbalance the inherent instability in the intestine, strategies such as co-administration of pH-modifying agents (like vitamin C) are sometimes used. These agents help to maintain a slightly acidic environment in the gut microenvironment, potentially improving EGCG stability during its transit and absorption.
– The use of acidifiers or buffering agents in supplements may help preserve EGCG until it reaches the absorption sites.

-Note half-life 3–5 hours.
- low BioAv 1%? despite its limited absorption, it is rapidly disseminated throughout the body
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Does NOT Lower AntiOxidant defense in Cancer Cells: NRF2↑, TrxR↓**, SOD, GSH Catalase HO1 GPx
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, Notch↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective(possible damage at high dose), CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Reactive oxygen species (ROS) ↑ ROS (dose-, metal-, context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation EGCG can act as a pro-oxidant in cancer cells (often metal-catalyzed) while functioning as an antioxidant in normal cells
2 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial stress and apoptosis follow ROS elevation in cancer cells
3 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of survival and inflammatory transcription NF-κB inhibition explains chemosensitization and reduced survival signaling
4 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ adaptive suppression Secondary Reduced growth and anabolic signaling AKT/mTOR inhibition contributes to growth suppression and stress responses
5 MAPK stress signaling (JNK / p38) ↑ JNK / ↑ p38 ↔ minimal Secondary Stress-activated apoptosis signaling MAPK activation often follows ROS increase and supports apoptotic signaling
6 Cell cycle regulation ↑ G1 or G2/M arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling disruption rather than direct CDK inhibition
7 HIF-1α / VEGF hypoxia–angiogenesis axis ↓ HIF-1α; ↓ VEGF ↔ minimal Secondary Anti-angiogenic pressure EGCG interferes with hypoxia-driven tumor adaptation
8 NRF2 antioxidant response ↑ NRF2 (adaptive, often insufficient) ↑ NRF2 (protective) Adaptive Stress compensation NRF2 reflects response to redox perturbation rather than a kill mechanism


Scientific Papers found: Click to Expand⟱
3235- EGCG,    (-)-Epigallocatechin-3-gallate reverses the expression of various tumor-suppressor genes by inhibiting DNA methyltransferases and histone deacetylases in human cervical cancer cells
- in-vivo, Cerv, HeLa
DNMTs↓, HDAC↓,
3236- EGCG,  BA,    Molecular mechanisms for inhibition of colon cancer cells by combined epigenetic-modulating epigallocatechin gallate and sodium butyrate
- in-vitro, Colon, RKO - in-vitro, Colon, HCT116 - in-vitro, Colon, HT29
Apoptosis↑, TumCCA?, HDAC1↓, DNMT1↓, survivin↓, HDAC↓, P21↑, NF-kB↑, γH2AX↑, ac‑H3↑, DNAdam↑,
3237- EGCG,    (-)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer's disease model mice by upregulating neprilysin expression
- in-vivo, AD, NA
*HDAC↓, *Aβ↓, cognitive↑,
3238- EGCG,    Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications
- Review, Var, NA
Telomerase↓, DNMTs↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, HATs↓, HDAC↓, selectivity↑, uPA↓, NF-kB↓, TNF-α↓, *ROS↓, *antiOx↑, Hif1a↓, VEGF↓, MMP2↓, MMP9↓, FAK↓, TIMP2↑, Mcl-1↓, survivin↓, XIAP↓, PCNA↓, p16↑, P21↑, p27↑, pRB↑, P53↑, MDM2↑, ROS↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Diablo↑, BAX⇅, cl‑PPARα↓, PDGF↓, EGFR↓, FOXO↑, AP-1↓, JNK↓, COX2↓, angioG↓,
3239- EGCG,    (−)-Epigallocatechin Gallate, A Major Constituent of Green Tea, Poisons Human Type II Topoisomerases
*TOP2↑,
3230- EGCG,    Green Tea Polyphenol Epigallocatechin 3-Gallate, Contributes to the Degradation of DNMT3A and HDAC3 in HCT 116 Human Colon Cancer Cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29
HDAC↓, DNMTs↓,
3241- EGCG,    Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
tumCV↓, mtDam↑, Apoptosis↑, ATP↓, lipoGen↓, eff↑,
3242- EGCG,    Epigallocatechin gallate has pleiotropic effects on transmembrane signaling by altering the embedding of transmembrane domains
ITGB3↓,
3243- EGCG,    (−)-Epigallocatechin-3-Gallate Inhibits Colorectal Cancer Stem Cells by Suppressing Wnt/β-Catenin Pathway
CD133↓, CSCs↓, TumCP↓, Apoptosis↑, Wnt↓, β-catenin/ZEB1↓,
3244- EGCG,    Novel epigallocatechin gallate (EGCG) analogs activate AMP-activated protein kinase pathway and target cancer stem cells
AMPK↑, TumCP↓, P21↑, mTOR↓, CSCs↓, CD44↓, CD24↓,
3245- EGCG,    (−)-Epigallocatechin-3-gallate protects PC12 cells against corticosterone-induced neurotoxicity via the hedgehog signaling pathway
- in-vitro, Nor, PC12
*neuroP↑, *Shh↑, *Gli1↑, *n-MYC↑, *Dose↝,
3246- EGCG,    Epigallocatechin gallate suppresses hepatic cholesterol synthesis by targeting SREBP-2 through SIRT1/FOXO1 signaling pathway
- in-vitro, Nor, NA
*MDA↓, *SOD↑, *SIRT1↑, *FOXO1↑, *SREBP2↓,
3428- EGCG,    Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein Complex
- Review, Var, NA
TumCCA↑, UHRF1↓, DNMT1↓, p16↑,
3591- EGCG,    Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in Rats
- in-vivo, AD, NA
*p‑tau↓, *BACE↓, *Aβ↓, *Ach↑, *AChE↓, *antiOx↑, *memory↑, *hepatoP↑, *ROS↓, *GPx↑, *SOD↑,
3221- EGCG,    EGCG upregulates phase-2 detoxifying and antioxidant enzymes via the Nrf2 signaling pathway in human breast epithelial cells
- in-vitro, Nor, MCF10
*antiOx↑, *GSTA1↑, *NRF2↑,
1036- EGCG,    Green Tea Catechin Is an Alternative Immune Checkpoint Inhibitor that Inhibits PD-L1 Expression and Lung Tumor Growth
- in-vitro, Lung, A549 - in-vitro, Lung, LU99
PD-L1↓, EGF↓, Akt↓,
3214- EGCG,    EGCG-induced selective death of cancer cells through autophagy-dependent regulation of the p62-mediated antioxidant survival pathway
- in-vitro, Nor, MRC-5 - in-vitro, Cerv, HeLa - in-vitro, Nor, HEK293 - in-vitro, BC, MDA-MB-231 - in-vitro, CRC, HCT116
mTOR↓, AMPK↑, selectivity↑, ROS↑, selectivity↑, HO-1↓, *NRF2↑, NRF2↓, *HO-1↑,
3215- EGCG,    Epigallocatechin gallate modulates ferroptosis through downregulation of tsRNA-13502 in non-small cell lung cancer
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, Ki-67↓, GPx4↓, ACSL4↑, Iron↑, MDA↑, ROS↑, Ferroptosis↑, eff↑, NRF2↑, HO-1↑,
3216- EGCG,    Epigallocatechin-3-gallate suppresses hemin-aggravated colon carcinogenesis through Nrf2-inhibited mitochondrial reactive oxygen species accumulation
- NA, Colon, Caco-2
NRF2↑, TumCP↓, mt-ROS↓, Keap1↓,
3217- EGCG,    Epigallocatechin-3-gallate promotes angiogenesis via up-regulation of Nfr2 signaling pathway in a mouse model of ischemic stroke
- in-vivo, Stroke, NA
*angioG↑, *neuroG↑, *NRF2↑,
3218- EGCG,    Comparative efficacy of epigallocatechin-3-gallate against H2O2-induced ROS in cervical cancer biopsies and HeLa cell lines
- in-vitro, Cerv, HeLa
SOD↑, GPx↑, *antiOx↑, ROS↓,
3219- EGCG,    Nano-chemotherapeutic efficacy of (−) -epigallocatechin 3-gallate mediating apoptosis in A549 cells: Involvement of reactive oxygen species mediated Nrf2/Keap1signaling
- in-vitro, Lung, A549
ROS↑, RNS↓, MMP↓, NRF2↑, Keap1↓,
3220- EGCG,    Dual Roles of Nrf2 in Cancer
- in-vitro, Lung, A549
NRF2↑, eff↓,
3212- EGCG,    EGCG maintained Nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cells
- in-vitro, Lung, A549 - in-vivo, Lung, NCIH23
NRF2⇅, eff↑, SOD1↑, SOD1↓, MMP2⇅, MMP9⇅,
3222- EGCG,    Epigallocatechin gallate and mitochondria—A story of life and death
- Review, Nor, NA
*lipid-P↓, *SOD↑, *Catalase↑, GPx↑, *GR↑, *GSTs↑, *GSH↑, *SIRT1↑, *PGC1A↑, *other↑,
3223- EGCG,    The Effects of Green Tea Catechins in Hematological Malignancies
- Review, AML, NA
Prx↓, ROS↑,
3224- EGCG,    Epigallocatechin-3-Gallate Prevents Acute Gout by Suppressing NLRP3 Inflammasome Activation and Mitochondrial DNA Synthesis
- in-vitro, Nor, NA
*Casp1↓, *NLRP3↓, *Inflam↓,
3225- EGCG,    Epigallocatechin‐3‐Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL‐1β Signaling Pathway
- in-vitro, Nor, NA - in-vivo, Nor, NA
*RenoP↑, *NLRP3↓, *TXNIP↓, *ASC↓, *Casp1↓, *IL1β↓, *ROS↓, *TNF-α↓, *IL6↓, *IL18↓,
3226- EGCG,    Epigallocatechin-3-gallate, a green-tea polyphenol, suppresses Rho signaling in TWNT-4 human hepatic stellate cells
- in-vitro, Nor, NA
*Rho↓, other↑,
3227- EGCG,    Epigallocatechin-3-gallate treatment to promote neuroprotection and functional recovery after nervous system injury
- NA, Nor, NA
*Rho↓, *IL1↓, *IL6↓, *TNF-α↓,
3228- EGCG,    Targeting fibrotic signaling pathways by EGCG as a therapeutic strategy for uterine fibroids
*cycD1/CCND1↓, *COL1A1↓, *ACTA2↓, *α-SMA↓,
3229- EGCG,    Epigallocatechin-3-gallate (EGCG) Alters Histone Acetylation and Methylation and Impacts Chromatin Architecture Profile in Human Endothelial Cells
- in-vitro, Nor, HMEC - in-vitro, Nor, HUVECs
HDAC↓,
658- EGCG,  MNPs,  MF,    Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio Interface
- in-vitro, GBM, LN229
*BioEnh↑,
649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, EGFR↓, HER2/EBBR2↓, IGF-1↓, MAPK↓, ERK↓, RAS↓, Raf↓, NF-kB↓, p‑pRB↓, TumCCA↑, Glycolysis↓, Warburg↓, HK2↓, Pyruv↓,
650- EGCG,    Cellular thiol status-dependent inhibition of tumor cell growth via modulation of retinoblastoma protein phosphorylation by (-)-epigallocatechin
- in-vitro, NA, NA
TumCCA↑, p‑pRB↓,
651- EGCG,    Epigallocatechin-3-Gallate Therapeutic Potential in Cancer: Mechanism of Action and Clinical Implications
ROS↑, p‑AMPK↑, mTOR↓, FAK↓, Smo↓, Gli1↓, HH↓, TumCMig↓, TumCI↓, NOTCH↓, JAK↓, STAT↓, Bcl-2↓, Bcl-xL↓, BAX↑, Casp9↑,
652- EGCG,  VitK2,  CUR,    Case Report of Unexpectedly Long Survival of Patient With Chronic Lymphocytic Leukemia: Why Integrative Methods Matter
- Case Report, CLL, NA
Remission↑,
653- EGCG,    Phase 2 Trial of Daily, Oral Polyphenon E in Patients with Asymptomatic, Rai Stage 0-II Chronic Lymphocytic Leukemia(CLL)
- Trial, CLL, NA
ALC↓, Remission↑,
654- EGCG,  MNPs,  MF,    Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potential
- in-vitro, Var, NA
*BioEnh↑,
655- EGCG,    A new molecular mechanism underlying the EGCG-mediated autophagic modulation of AFP in HepG2 cells
- in-vitro, HCC, HepG2
AFP↓, TumAuto↑, LC3II↑, TumCG↓, MMP↓,
657- EGCG,  MNPs,  MF,    Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cells
- in-vitro, GBM, U87MG
*BioEnh↑,
648- EGCG,    Bioavailability of Epigallocatechin Gallate Administered With Different Nutritional Strategies in Healthy Volunteers
- Human, Nor, NA
*BioAv↑,
659- EGCG,  MNPs,  MF,    Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interaction
- in-vivo, Nor, NA
*BioEnh↑,
660- EGCG,  FA,    Epigallocatechin-3-gallate Delivered in Nanoparticles Increases Cytotoxicity in Three Breast Carcinoma Cell Lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
Apoptosis↑, *toxicity↓, *eff↓,
661- EGCG,  GoldNP,    Epigallocatechin-3-Gallate-Loaded Gold Nanoparticles: Preparation and Evaluation of Anticancer Efficacy in Ehrlich Tumor-Bearing Mice
- vitro+vivo, NA, NA
Apoptosis↑, TumVol↓,
662- EGCG,    Advanced Nanovehicles-Enabled Delivery Systems of Epigallocatechin Gallate for Cancer Therapy
- Review, Var, NA
*BioEnh↑,
663- EGCG,    EGCG-coated silver nanoparticles self-assemble with selenium nanowires for treatment of drug-resistant bacterial infections by generating ROS and disrupting biofilms
- in-vitro, NA, NA
ROS↑,
664- EGCG,  AgNPs,    Epigallocatechin-3-gallate-capped Ag nanoparticles: preparation and characterization
- Analysis, NA, NA
other↑,
1056- EGCG,    EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression
- vitro+vivo, BC, E0771
TumW↓, VEGF↓, Weight∅, Hif1a↓, NF-kB↓,
666- EGCG,    The Role of EGCG in Breast Cancer Prevention and Therapy
- Review, NA, NA
ROMO1↑, VEGF↓, TumCG↓,

Showing Research Papers: 51 to 100 of 174
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 174

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx↑, 2,   GPx4↓, 1,   HO-1↓, 1,   HO-1↑, 1,   Iron↑, 1,   Keap1↓, 2,   MDA↑, 1,   NRF2↓, 1,   NRF2↑, 4,   NRF2⇅, 1,   Prx↓, 1,   RNS↓, 1,   ROMO1↑, 1,   ROS↓, 1,   ROS↑, 7,   mt-ROS↓, 1,   SOD↑, 1,   SOD1↓, 1,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   EGF↓, 1,   MMP↓, 2,   mtDam↑, 1,   Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   AMPK↑, 2,   p‑AMPK↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   lipoGen↓, 1,   cl‑PPARα↓, 1,   Pyruv↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 5,   BAX↑, 1,   BAX⇅, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   Diablo↑, 1,   Ferroptosis↑, 1,   JNK↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   MDM2↑, 1,   p27↑, 1,   survivin↓, 2,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   HATs↓, 1,   other↑, 2,   pRB↑, 1,   p‑pRB↓, 2,   tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 2,   DNMTs↓, 3,   p16↑, 2,   P53↑, 1,   PCNA↓, 1,   UHRF1↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 3,   TumCCA?, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD24↓, 1,   CD44↓, 1,   CSCs↓, 2,   ERK↓, 1,   FOXO↑, 1,   Gli1↓, 1,   HDAC↓, 5,   HDAC1↓, 1,   HH↓, 1,   IGF-1↓, 1,   mTOR↓, 3,   NOTCH↓, 1,   RAS↓, 1,   Smo↓, 1,   STAT↓, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   FAK↓, 2,   ITGB3↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP2⇅, 1,   MMP9↓, 1,   MMP9⇅, 1,   PDGF↓, 1,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   uPA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,   Hif1a↓, 2,   VEGF↓, 3,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   JAK↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   PD-L1↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 3,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

AFP↓, 1,   ALC↓, 1,   EGFR↓, 2,   HER2/EBBR2↓, 1,   Ki-67↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   Remission↑, 2,   TumVol↓, 1,   TumW↓, 1,   Weight∅, 1,  
Total Targets: 136

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTA1↑, 1,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 3,   ROS↓, 3,   SOD↑, 3,  

Core Metabolism/Glycolysis ⓘ

PGC1A↑, 1,   SIRT1↑, 2,   SREBP2↓, 1,  

Cell Death ⓘ

Casp1↓, 2,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO1↑, 1,   Gli1↑, 1,   HDAC↓, 1,   n-MYC↑, 1,   neuroG↑, 1,   Shh↑, 1,   TOP2↑, 1,  

Migration ⓘ

ACTA2↓, 1,   COL1A1↓, 1,   Rho↓, 2,   TXNIP↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   IL1↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL6↓, 2,   Inflam↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 2,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioEnh↑, 6,   Dose↝, 1,   eff↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 2,  

Functional Outcomes ⓘ

hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 55

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:73  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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